One response to inhaled noxious aerosols is an abrupt termination of inspiration. This reflex is elicited by the branch of trigeminal nerve that innervates the nasal mucosa. If irritants persist in the upper airway or enter the lower airway, then more complex changes occur in the breathing pattern. Central mechanisms forming these integrated responses, especially those elicited by the trigeminal nerve, are poorly understood. We hypothesize that the pontine respiratory group (PRG), a bilateral structure in the rostral, dorso- lateral pons, is a major nucleus necessary for the incorporation of sensory stimuli into the central pattern generator for respiration. Specifically, we believe that the PRG shapes the breathing pattern in response to stimulation of the nasal mucosal, laryngeal, and intrathoracic airway receptors. Furthermore, we hypothesize that PRG neurons that are poorly correlated with respiration are more responsive to sensory stimulation and are more sensitive to changes in state of consciousness than those neurons whose activity is highly modulated by respiration. We propose a set of neurophysiologic experiments in both anesthetized and unanesthetized cats to determine if airway afferent and PRG activities terminate inspiration through post-inspiratory neurons and if more complex reshaping of the breathing pattern is dependent on the PRG. We will record inspiratory, expiratory and post-inspiratory motor unit activity and compare their responses to stimulation of trigeminal and superior laryngeal nerves before and after injection of cobalt in the PRG. We will stimulate subregions of the PRG chemically and electrically and record short-latency responses of medullary post-inspiratory neuronal and respiratory muscle activity and of respiratory timing (TI,TE,TTOT). We will use quantitative methods for determining the relationship between recorded PRG neural activity and respiration. This correlation reflects a balance between respiratory and non-respiratory synaptic drive to a neuron. A weakly correlated and poorly modulated cell reflects a predominance of non-respiratory inputs. The aims are to: 1) compare the muscle and timing responses to airway-afferent stimulation before and after blocking synaptic transmission in the PRG, 2) determine the pattern of respiratory muscle activity elicited by microstimulation of the PRG, 3) analyze the activity patterns of PRG neurons and correlate their behavior to their responses to afferent stimulation and to changes in state of consciousness and 4) analyze the response of medullary post- inspiratory neurons, neurons that are excited by superior laryngeal nerve stimulation, to trigeminal nerve and PRG stimulation. Results will provide insight into the neurophysiologic mechanisms for influence of PRG and airway afferent information on medullary stimulation, weakly and strongly modulated PRG neurons, and medullary post-inspiratory neurons. Such interaction may be relevant to understanding changes in the breathing pattern with activation of upper and lower airway afferent nerves during inflammation and irritation.